Institution
Northwestern University
Education•Evanston, Illinois, United States•
About: Northwestern University is a education organization based out in Evanston, Illinois, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 75430 authors who have published 188857 publications receiving 9463252 citations. The organization is also known as: Northwestern & NU.
Topics: Population, Medicine, Cancer, Health care, Transplantation
Papers published on a yearly basis
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TL;DR: In this paper, the authors confirm the presence of a unit root in the autoregressive polynomial of the univariate time series representation of daily exchange-rate data and show that the first differences of the logarithms of daily spot rates are approximately uncorrelated through time.
Abstract: Formal testing procedures confirm the presence of a unit root in the autoregressive polynomial of the univariate time series representation of daily exchange-rate data. The first differences of the logarithms of daily spot rates are approximately uncorrelated through time, and a generalized autoregressive conditional heteroscedasticity model with daily dummy variables and conditionally t-distributed errors is found to provide a good representation to the leptokurtosis and time-dependent conditional heteroscedasticity. The parameter estimates and characteristics of the models are found to be very similar for six different currencies. These apparent stylized facts carry over to weekly, fortnightly, and monthly data in which the degree of leptokurtosis and time-dependent heteroscedasticity is reduced as the length of the sampling interval increases.
1,002 citations
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TL;DR: Superconducting circuits exhibit behavior analogues to natural quantum entities, such as atom, ions and photons as mentioned in this paper, and large-scale arrays of such circuits hold the promise of providing a unique route to quantum simulation.
Abstract: Lithographically fabricated micrometre-scale superconducting circuits exhibit behaviour analogues to natural quantum entities, such as atom, ions and photons. Large-scale arrays of such circuits hold the promise of providing a unique route to quantum simulation. Recent progress in technology and methodology are reviewed here, and prospects and challenges discussed.
1,002 citations
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TL;DR: A concise user guide is presented outlining the steps required to obtain thermodynamic information from ab initio calculations of alloy thermodynamic properties from first-principles.
Abstract: Although the formalism that allows the calculation of alloy thermodynamic properties from
first-principles has been known for decades, its practical implementation has so far remained a tedious
process. The Alloy Theoretic Automated Toolkit (ATAT) drastically simplifies this procedure by implementing
decision rules based on formal statistical analysis that frees the researchers from a constant
monitoring during the calculation process and automatically “glues” together the input and the output of
various codes, in order to provide a high-level interface to the calculation of alloy thermodynamic properties
from first-principles. ATAT implements the Structure Inversion Method (SIM), also known as the
Connolly-Williams method, in combination with semi-grand-canonical Monte Carlo simulations. In order
to make this powerful toolkit available to the wide community of researchers who could benefit from it,
this article present a concise user guide outlining the steps required to obtain thermodynamic information
from ab initio calculations.
1,001 citations
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Memorial Hospital of South Bend1, Howard University2, Northwestern University3, George Washington University4, Harvard University5, Stanford University6, Yeshiva University7, University of Pittsburgh8, Fred Hutchinson Cancer Research Center9, University of California, San Diego10, Rutgers University11, University of Alabama at Birmingham12, University of Florida13, University of Minnesota14, Ohio State University15, University of Massachusetts Medical School16, University of Miami17, Emory University18, University of California, Davis19, National Institutes of Health20, University of Wisconsin-Madison21, University of Iowa22, Kaiser Permanente23, University at Buffalo24, Wake Forest University25, Brown University26, Pfizer27, University of Arizona28, Rush University Medical Center29, University of Nevada, Reno30, University of Texas at San Antonio31, University of California, Los Angeles32, University of Cincinnati33, Stony Brook University34, Baylor College of Medicine35, University of North Carolina at Chapel Hill36, Wayne State University37, University of California, Irvine38, University of Tennessee Health Science Center39, Medical College of Wisconsin40
TL;DR: A dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVDrisk.
Abstract: ContextMultiple epidemiologic studies and some trials have linked diet with cardiovascular disease (CVD) prevention, but long-term intervention data are needed.ObjectiveTo test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk.Design, Setting, and ParticipantsRandomized controlled trial of 48 835 postmenopausal women aged 50 to 79 years, of diverse backgrounds and ethnicities, who participated in the Women's Health Initiative Dietary Modification Trial. Women were randomly assigned to an intervention (19 541 [40%]) or comparison group (29 294 [60%]) in a free-living setting. Study enrollment occurred between 1993 and 1998 in 40 US clinical centers; mean follow-up in this analysis was 8.1 years.InterventionIntensive behavior modification in group and individual sessions designed to reduce total fat intake to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received diet-related education materials.Main Outcome MeasuresFatal and nonfatal coronary heart disease (CHD), fatal and nonfatal stroke, and CVD (composite of CHD and stroke).ResultsBy year 6, mean fat intake decreased by 8.2% of energy intake in the intervention vs the comparison group, with small decreases in saturated (2.9%), monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d). Low-density lipoprotein cholesterol levels, diastolic blood pressure, and factor VIIc levels were significantly reduced by 3.55 mg/dL, 0.31 mm Hg, and 4.29%, respectively; levels of high-density lipoprotein cholesterol, triglycerides, glucose, and insulin did not significantly differ in the intervention vs comparison groups. The numbers who developed CHD, stroke, and CVD (annualized incidence rates) were 1000 (0.63%), 434 (0.28%), and 1357 (0.86%) in the intervention and 1549 (0.65%), 642 (0.27%), and 2088 (0.88%) in the comparison group. The diet had no significant effects on incidence of CHD (hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI, 0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05). Excluding participants with baseline CVD (3.4%), the HRs (95% CIs) for CHD and stroke were 0.94 (0.86-1.02) and 1.02 (0.90-1.17), respectively. Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.ConclusionsOver a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors, suggesting that more focused diet and lifestyle interventions may be needed to improve risk factors and reduce CVD risk.Clinical Trials RegistrationClinicalTrials.gov Identifier: NCT00000611
1,000 citations
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Washington University in St. Louis1, Northwestern University2, University of British Columbia3, Ludwig Maximilian University of Munich4, University of Pennsylvania5, University of Texas Southwestern Medical Center6, Rush University Medical Center7, University of São Paulo8, Neuroscience Research Australia9, University of Paris10, Queen's University11, Aalborg University12, University of Basel13, Gunma University14, University of Ottawa15, University of Toronto16, Mayo Clinic17, University of Sheffield18, University of Manchester19
TL;DR: The aim of this study was to improve the neuropathologic recognition and provide criteria for the pathological diagnosis in the neurodegenerative diseases grouped as frontotemporal lobar degeneration (FTLD) and incorporate up-to-date neuropathology in the light of recent immunohistochemical, biochemical, and genetic advances.
Abstract: The aim of this study was to improve the neuropathologic recognition and provide criteria for the pathological diagnosis in the neurodegenerative diseases grouped as frontotemporal lobar degeneration (FTLD); revised criteria are proposed. Recent advances in molecular genetics, biochemistry, and neuropathology of FTLD prompted the Midwest Consortium for Frontotemporal Lobar Degeneration and experts at other centers to review and revise the existing neuropathologic diagnostic criteria for FTLD. The proposed criteria for FTLD are based on existing criteria, which include the tauopathies [FTLD with Pick bodies, corticobasal degeneration, progressive supranuclear palsy, sporadic multiple system tauopathy with dementia, argyrophilic grain disease, neurofibrillary tangle dementia, and FTD with microtubule-associated tau (MAPT) gene mutation, also called FTD with parkinsonism linked to chromosome 17 (FTDP-17)]. The proposed criteria take into account new disease entities and include the novel molecular pathology, TDP-43 proteinopathy, now recognized to be the most frequent histological finding in FTLD. TDP-43 is a major component of the pathologic inclusions of most sporadic and familial cases of FTLD with ubiquitin-positive, tau-negative inclusions (FTLD-U) with or without motor neuron disease (MND). Molecular genetic studies of familial cases of FTLD-U have shown that mutations in the progranulin (PGRN) gene are a major genetic cause of FTLD-U. Mutations in valosin-containing protein (VCP) gene are present in rare familial forms of FTD, and some families with FTD and/or MND have been linked to chromosome 9p, and both are types of FTLD-U. Thus, familial TDP-43 proteinopathy is associated with defects in multiple genes, and molecular genetics is required in these cases to correctly identify the causative gene defect. In addition to genetic heterogeneity amongst the TDP-43 proteinopathies, there is also neuropathologic heterogeneity and there is a close relationship between genotype and FTLD-U subtype. In addition to these recent significant advances in the neuropathology of FTLD-U, novel FTLD entities have been further characterized, including neuronal intermediate filament inclusion disease. The proposed criteria incorporate up-to-date neuropathology of FTLD in the light of recent immunohistochemical, biochemical, and genetic advances. These criteria will be of value to the practicing neuropathologist and provide a foundation for clinical, clinico-pathologic, mechanistic studies and in vivo models of pathogenesis of FTLD.
1,000 citations
Authors
Showing all 76189 results
Name | H-index | Papers | Citations |
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George M. Whitesides | 240 | 1739 | 269833 |
Ralph B. D'Agostino | 226 | 1287 | 229636 |
Daniel Levy | 212 | 933 | 194778 |
David Miller | 203 | 2573 | 204840 |
Ronald M. Evans | 199 | 708 | 166722 |
Michael Marmot | 193 | 1147 | 170338 |
Robert C. Nichol | 187 | 851 | 162994 |
Scott M. Grundy | 187 | 841 | 231821 |
Stuart H. Orkin | 186 | 715 | 112182 |
Michael A. Strauss | 185 | 1688 | 208506 |
Ralph Weissleder | 184 | 1160 | 142508 |
Patrick O. Brown | 183 | 755 | 200985 |
Aaron R. Folsom | 181 | 1118 | 134044 |
Valentin Fuster | 179 | 1462 | 185164 |
Ronald C. Petersen | 178 | 1091 | 153067 |